1. Field of the Invention
This invention relates to methods and devices for analysis of the electrical activity of the heart (Electrocardiography) and more particularly to the field known as High Resolution Electrocardiography, which is concerned with detecting abnormalities not apparent on conventional electrocardiograms. The specific and major purpose intended for the present invention is the clinical evaluation of medical patients for risk of life-threatening arrhythmias of the heart. However, both the method and apparatus are potentially suitable for research into and diagnosis of a wide variety of other disorders of cardiac electrical activity, and the analysis of other bioelectrical signals such as those recorded on an Electroencephalogram (EEG).
2. Description of the Prior Art
In order to fully comprehend the purpose and method of the present invention, it is necessary to be familiar with certain standard physiological and electrocardiographic (ECG) nomenclature. Relevant portions of that nomenclature are briefly summarized here for the benefit of the reader not conversant with medical terminology.
The pumping action of the normal heart results from the orderly contraction of millions of individual muscle cells. Each heart beat is initiated by the spontaneous periodic activity of certain specialized cells of a structure known as the sino-atrial node. Activation of heart muscle cells is initiated by an electrical pacing signal generated in the sino-atrial node and propagated by specialized tissues known collectively as "the conducting system" of the heart. At the cellular level, the process of activation is known as "depolarization" because it involves transient changes in the electrical potential across the cell membrane mediated by the passage of ions. The process of recovery to the normal resting state is referred to as "repolarization".
The spread of the wavefront of electrical depolarization through the atria, that is the "primer pumping chambers" of the heart, gives rise to the deflection on the electrocardiogram known as the P wave. Contraction of the main cardiac pumping chambers, that is the ventricles of the heart, is associated with a multiphasic deflection of the ECG waveform known as the QRS complex. Spread of the wavefront of electrical recovery (repolarization) through the ventricles gives rise to the T wave of the ECG. The time interval between the end of the QRS complex and the T wave, referred to as the ST segment, is normally free from electrical activity, but may harbor small amplitude signals known as late potentials which extend out beyond the end of the QRS complex (as viewed at ordinary magnification) into the ST segment. All of the components of ECG waveforms result from the synchronous spread of electrical signals associated with the activation or recovery of individual cardiac cells, across millions of such cells.
Over fifty-thousand people die annually in the U.S. of unexpected or sudden cardiac death, almost always from a catastrophic failure of normal electrical conduction within the heart known as ventricular fibrillation. Instead of the normal orderly and synchronous contraction of the heart muscle cells necessary for pumping of blood to occur, individual muscle fibers contract in a random and totally disorganized fashion. This arrhythmia (abnormal cardiac rhythm) frequently occurs in association with a myocardial infarction, i.e. a heart attack, either within the first minutes, hours, or sometimes months to years later, but is also the final common pathway for almost all forms of death from cardiac causes. Ventricular fibrillation is a terminal event because no blood at all gets pumped and vital organs such as the brain die from lack of oxygen within minutes unless either the rhythm is corrected, i.e. defibrillated, or the circulation is artificially supported by some other means such as CPR or cardiopulmonary bypass (heart-lung machine).
A frequent immediate predecessor to ventricular fibrillation is another arrhythmia known as ventricular tachycardia (VT) during which, although some blood is pumped, the heart rate is usually too rapid for efficient pumping to occur. The resulting decrease in blood flow may result in symptoms such as loss of consciousness or lightheadedness. VT may spontaneously revert back to a more normal heart rhythm in which case it is referred to as "nonsustained", or it may persist for longer than thirty seconds in which case it is referred to as "sustained". If all QRS complexes during an episode of VT appear similar to each other, the VT is referred to as "monomorphic". Sustained monomorphic ventricular tachycardia (SMVT) has been shown to be closely linked with risk of sudden death in clinical studies.
Despite the existence of a wide variety of more or less successful treatments such as drug therapy, surgery or implantable defibrillators for the prevention or correction of ventricular arrhythmias, their use is not without risk or expense. Classical electrocardiography as practiced for several decades is unfortunately very poor at predicting who is likely to suffer ventricular arrhythmias. Although it is known that increased risk is associated with certain states such as a severely damaged or dilated left ventricle, (the main pumping chamber of the heart), there remains an urgent need for a means of delineating those patients at significant risk, who might truly benefit from aggressive therapies, from amongst the vast majority of potential candidates in whom the risk of life threatening arrhythmia is low and for whom aggressive or expensive therapies may actually do more harm than good. Such an arrhythmia risk screening test should preferably be non-invasive, i.e., not require breaking of the skin surface, and free from risk and discomfort to the patient.
The most reliable method currently available for predicting likelihood of development of a lethal arrhythmia is a diagnostic procedure called electrophysiological study (EP), during which slender wires referred to as pacing catheters are introduced through the skin into a large vein and advanced under X-ray guidance into the heart chambers. Attached to the pacing catheters is a device which generates electrical pulses similar to those produced by a pacemaker. The interior surface of the heart is then subjected to electrical stimulation pulses in an attempt to induce sustained monomorphic ventricular tachycardia. If SMVT is successfully induced, the patient is deemed to be much more likely to spontaneously develop a lethal rhythm disorder. Unfortunately, electrophysiological study is invasive, requires admitting the patient to hospital, is often distressing to the patient who may have to be defibrillated out of a successfully induced arrhythmia, and is time, labor and cost intensive.
Among available non-invasive arrhythmia risk assessment techniques, so-called late potential analysis has received the most attention both in the medical literature and commercial practice. The patents of Simpson, U.S. Pat. No. 4,422,459, Netravali, U.S. Pat. No. 4,458,691, and Strick, U.S. Pat. No. 4,492,235, teach a method currently in widespread use on real-time ECG recorders. Many variants of the method have been advocated in the medical literature. Late potentials are signals of very low amplitude, i.e. less than forty micro volts, versus about one milli volt for the main QRS signal, and, thus require employment of a special noise reduction technique known as signal averaging for such late potentials to be discernible above background noise. Late potential presence beyond the end of the normal QRS 4 complex is about seventy percent predictive for inducibility of SMVT at electrophysiological study and thus predictive of possible serious spontaneous ventricular arrhythmia. However, late potential analysis cannot be used at all in the presence of certain relatively common types of ECG abnormality, and its sensitivity is less than would be desirable.
The Simson patent teaches identification of late potentials by analysis in the time domain only, without any attempt to explicitly analyze their frequency spectral content. Bipolar ECG signals from three orthogonal surface leads are bidirectionally filtered and then algebraically summed into a single vector magnitude upon which certain characteristics of the terminal QRS signal are then measured. Late potentials are deemed to be present or absent depending upon the duration and amplitude of the terminal QRS region. Late potentials are sometimes found by time domain techniques in perfectly normal, healthy patients. The present invention teaches a method which has been shown in clinical studies to be substantially more accurate than late potential analysis at correctly identifying patients in whom SMVT would be inducible at electrophysiologic study, and hence are at increased risk of life- threatening arrhythmia.
The Kelen U.S. Pat. No. 4,883,065, disclosed a system for the analysis of late potentials from long-term recordings of ECGs made on an ambulatory monitor, e.g. a Holter monitor.
The Ambos et al US Pat. No. 4,680,708, teaches a frequency domain technique for late potential identification using Fourier analysis of a single, relatively long segment of ECG signal positioned over the terminal QRS region. Abnormality is allegedly characterized by the presence of secondary high frequency peaks and an excess ratio of high frequencies to low frequencies.
Frequency spectral analysis techniques for ventricular tachycardia risk assessment have, prior to the present invention, used Fourier Analysis of the terminal portion of the QRS complex and early ST segment seeking to identify late potentials by unique frequency spectral content in the form of additional high frequency peaks or abnormal content of high frequencies. These techniques have sought to improve tachyarrhythmia risk detection by better identification of late potentials based upon their putative frequency characteristics. These techniques have been criticized as unreproducible and unconfirmed by independent research. A serious theoretical limitation of late potential analysis arises from the concept that these potentials may represent the visible tip of large but obscured myocardial regions with abnormal activation having most of the electrical activity from such regions buried partially or totally within the QRS complex proper. Partial obscuring of late potentials may occur if the abnormal myocardial region begins to be activated relatively early during the QRS complex, for example, in anterior as compared to inferior wall myocardial infarction. During bundle branch block, myocardial zones with abnormal activation may be totally obscured by the delayed activation of normal myocardial regions. On the other hand, time domain analysis may show late potentials in otherwise normal hearts as a result of applying a high pass filter to a terminal QRS region of lower than normal amplitude or slope due to bundle branch block.
Other limitations of time domain analysis include sensitivity to the specific algorithm used for determining QRS termination, the arbitrary nature of the scoring criteria, and the relatively low predictive accuracy of late potential analysis in the presence of intraventricular conduction defect or bundle branch block. Conventional frequency domain analysis as practiced by the prior art is vulnerable to the duration and the time phase of the analyzed signal as well as to the arbitrary definition of low and high frequency components of the signals.
Hence there exists a need to more accurately predict those at risk from ventricular arrhythmias. The limitations and disadvantages of the prior art are solved or reduced by employing the systems and methods of present invention.